The development of synaptically active networks of mammalian central neurons has been studied in dissociated cell cultures by intracellular microelectrode and light and electron microscopic techniques. Chronic treatment of spinal cord cultures with glycine produces a defect in inhibitory synaptic action with consequent paroxysmal activity of the cultures. GABA treatment, by contrast, produces quiescent neural networks, probably by a presynaptic inhibitory mechanism. Excitatory synaptic activity is not mediated by glutamate, a potent excitatory amino acid. Injection of a marker enzyme, horseradish peroxidase, allows identification of all ramifications of intracellularly recorded or stimulated neurons. This has allowed morpho-physiologic correlative study at the electron microscopic level of excitatory and inhibitory synapses. BIBLIOGRAPHIC REFERENCE: Ransom, B.R. and Nelson, P.G.: Possible pathophysiology of neurologic abnormalities associated with nonketotic hyperglycemia. Letters, N. Eng. J. Med. 294: 1295-1296, 1976.